Syn-Coll

Dosing from the Literature

Published for skin: the supplier's own tests — creams with 10–25 ppm of the peptide, and a cream applied twice daily for 84 days by 60 volunteers (Schagen, 2017); its product page also cites four-week tests of 1%, 2.5% and 5% of its Syn-Coll CB solution (dsm-firmenich product page). Not published: a peer-reviewed report of any of these trials.

Syn-Coll "dosing" is a formulation parameter, not a clinical dose. The levels below are those the supplier reports testing; its product page and safety data sheet do not state how much peptide its solution contains.

What It Is

Syn-Coll is a lipopeptide consisting of the tripeptide (a chain of 3 amino acids) sequence L-Lysine–L-Valine–L-Lysine N-terminally conjugated to palmitic acid (hexadecanoic acid). Its INCI name is Palmitoyl Tripeptide-5; older labels occasionally list it as "Palmitoyl Tripeptide-3" after an earlier INCI numbering that the International Nomenclature of Cosmetic Ingredients reassigned. The molecular formula is C₃₃H₆₅N₅O₅ and the molecular weight is approximately 611.9 Da. The palmitoyl group is what converts an otherwise hydrophilic, barrier-excluded tripeptide into a lipophilic anchor capable of partitioning into the stratum corneum and reaching live epidermis and upper dermis on topical application. The raw peptide itself (Lys-Val-Lys, tripeptide-5) is unremarkable in cosmetic assays; the commercial ingredient is always the palmitoylated form.

Syn-Coll was developed and commercialized by Pentapharm Ltd. (Basel, Switzerland), a longtime supplier of active cosmetic ingredients. Pentapharm was acquired by DSM Nutritional Products in 2007, and the Syn-Coll trademark now sits in DSM's Personal Care portfolio. DSM supplies it as a glycerin-based water solution (glycerol 50–70%; DSM safety data sheet, 2017); its 2024 product page described the solution as containing no intentionally added preservative (dsm-firmenich product page, 2024 version). Its current product page reports tests of 1%, 2.5% and 5% of its newer version, Syn-Coll CB, in finished products (dsm-firmenich product page). Neither document states how much peptide the solution holds; a cream used in the supplier's wrinkle test contained 10–25 ppm of the peptide (Schagen, 2017).

The compound is used exclusively topically. It is not a research peptide intended for systemic administration by any route, and there is no published pharmacokinetic or safety data supporting subcutaneous, intramuscular, intravenous, intranasal, or oral use. Unlike peptides such as BPC-157, GHK-Cu (in its systemic context), or GHRP-class compounds, Syn-Coll has no legitimate "research chemical" systemic application — it is a cosmetic signal molecule from inception. Any vendor offering Syn-Coll for injection is selling a topical ingredient out of its intended regulatory class.

Regulatory classification places Syn-Coll firmly in the cosmetic-ingredient universe, not the drug universe. In the United States it is a permitted cosmetic ingredient under the FD&C Act definition of a cosmetic (articles intended for cleansing, beautifying, or altering appearance), and in the European Union it is listed in the CosIng database of cosmetic ingredients. Neither jurisdiction has approved it as a drug for any indication, and cosmetic-labeling rules prohibit claims that it "treats," "cures," or "prevents" any disease or structurally alters the skin in a way that would trigger drug classification.

The clinical evidence base for Syn-Coll — as distinct from the evidence base for the underlying TSP-1/TGF-β activation biology — is limited and substantially manufacturer-sponsored. PubMed does not index independent randomized controlled trials of Syn-Coll as a monotherapy against vehicle using rigorous wrinkle-morphometry endpoints. The strongest evidence in the peer-reviewed cosmetic-science literature is narrative review-chapter coverage; the strongest individual data points are supplier-issued technical bulletins and conference abstracts. This is typical of the cosmetic active-ingredient category, but it is an important honest framing for a site that reviews peptides by evidence quality.

Mechanism of Action

Syn-Coll is pitched as a mimic of one well-studied pathway: thrombospondin-1 (TSP-1) activating latent TGF-β without cutting it (Schagen, 2017; Murphy-Ullrich & Suto, 2018). Its maker says the tripeptide reproduces that step, mimicking the body's own activation of latent TGF-β (dsm-firmenich product page, 2024 version). Key mechanistic points:

• Latent TGF-β biology — TGF-β is secreted by virtually all cells in a latent form (Schultz-Cherry et al., 1995). In the small latent complex (SLC), the mature TGF-β homodimer is held non-covalently by its own propeptide, the latency-associated peptide (LAP), which binds its receptor-binding region (Young & Murphy-Ullrich, 2004; PMID 15208302; Murphy-Ullrich & Suto, 2018). In the large latent complex (LLC), the SLC is also bound to the fibrillin-like latent TGF-β binding protein (LTBP) (Murphy-Ullrich & Suto, 2018). For TGF-β to signal, the mature domain must be released from LAP — a step that is tightly regulated because unchecked TGF-β signaling drives fibrosis and scarring (Murphy-Ullrich & Poczatek, 2000; Murphy-Ullrich & Suto, 2018).
• TSP-1 as a latent-TGF-β activator — Thrombospondin-1 is a matricellular protein found in platelet α-granules and in the extracellular matrix (Schultz-Cherry et al., 1994; PMID 7929413; Murphy-Ullrich & Suto, 2018). Schultz-Cherry and Murphy-Ullrich (1993, J Cell Biol; PMID 8349738) first showed that TSP-1 stripped of co-associated TGF-β can non-proteolytically activate latent TGF-β secreted by endothelial cells. Crawford et al. (1998, Cell; PMID 9657149) then demonstrated in TSP-1-null mice that TSP-1 is responsible for a physiologically significant fraction of latent TGF-β1 activation in vivo, with overlapping organ-system phenotypes between TGF-β1-null and TSP-1-null animals.
• The KRFK activation motif — The activation activity of TSP-1 maps to its three type-1 thrombospondin repeats (TSRs) (Schultz-Cherry et al., 1994; PMID 7929414). Within the TSRs, Schultz-Cherry et al. (1995, J Biol Chem; PMID 7706271) identified the four-residue sequence KRFK (Lys-Arg-Phe-Lys), positioned between the first and second type-1 repeats, as the motif responsible for latent-TGF-β activation. Synthetic KRFK-containing peptides also activate latent TGF-β, as TSP-1 does (Ribeiro et al., 1999).
• LAP as the docking target — Ribeiro et al. (1999, J Biol Chem; PMID 10224129) mapped the reciprocal binding site on the LAP: the N-terminal LSKL sequence of the latency-associated peptide directly interacts with the TSP-1 KRFK motif. LSKL also binds the RKPK sequence in the receptor-binding region of mature TGF-β, which keeps it latent; KRFK binding to LSKL competitively disrupts that contact and displaces LAP, so active TGF-β is released without proteolytic cleavage (Young & Murphy-Ullrich, 2004; PMID 15208302; Murphy-Ullrich & Suto, 2018). Synthetic LSKL peptides competitively block activation by TSP-1 or KRFK peptides (Ribeiro et al., 1999).
• Syn-Coll as a claimed KRFK mimic (Pal-KVK) — A review describes palmitoyl tripeptide-5 (Pal-Lys-Val-Lys) as mimicking TSP-1, whose Lys-Arg-Phe-Lys sequence is responsible for its TGF-β stimulation (Schagen, 2017). Compared with KRFK, the K-V-K core keeps the two end lysines and has a single valine in place of arginine–phenylalanine. Its maker says it boosts collagen by mimicking the body's own mechanism for activating latent TGF-β (dsm-firmenich product page, 2024 version). No published study outside the supplier has tested whether Pal-KVK binds LAP or activates latent TGF-β.
• Downstream TGF-β / SMAD signaling — Once released, active TGF-β binds its signaling receptors and signals through Smad proteins (Murphy-Ullrich & Suto, 2018). In normal human dermal fibroblasts it causes "a persistent increase in steady-state amounts of type I and type III collagen and fibronectin mRNAs" (Varga, Rosenbloom & Jimenez, 1987, Biochem J; PMID 3501287), building on earlier work showing that TGF-β raises fibronectin and collagen expression (Ignotz & Massagué, 1986).
• Anti-MMP / anti-collagenase claim — Its maker says Syn-Coll also protects collagen from degradation by inhibiting matrix metalloproteinases (dsm-firmenich product page, 2024 version), and a review reports in-vitro results against MMP-1 (interstitial collagenase) and MMP-3 (stromelysin-1) (Schagen, 2017). No independent study has tested this for Pal-KVK; for a related lipid-linked tripeptide, elaidyl-KFK, fibroblast tests showed more collagen and TIMP-1 (tissue inhibitor of metalloproteinases-1) and less MMP-1 (Errante et al., 2020).
• Palmitoyl moiety — The unmodified Lys-Val-Lys tripeptide is short (MW ≈ 373 Da). N-terminal conjugation of palmitic acid (a C16 saturated fatty acid) is the same strategy used for Matrixyl (palmitoyl pentapeptide-4, Pal-KTTKS), palmitoyl tripeptide-1 (Pal-GHK) and palmitoyl tetrapeptide-7 (Pal-GQPR): a review reports that for Pal-KTTKS the palmitoyl tail gives more effective delivery across the skin and better stability to skin proteases, and that Pal-GHK was designed to improve stability and transdermal delivery (Errante et al., 2020). The review gives no such data for Pal-KVK.
• What is and is not established — Established in cell and mouse studies: TSP-1 activates latent TGF-β through its KRFK sequence binding LAP's LSKL sequence (Ribeiro et al., 1999; Crawford et al., 1998), and TGF-β raises type I and III collagen and fibronectin in human dermal fibroblasts (Varga et al., 1987). Not tested outside the supplier: whether Pal-KVK activates latent TGF-β at cosmetic levels in living human skin.

What the Research Shows

Research on Syn-Coll falls into three tiers: (1) foundational TSP-1 / TGF-β biology, which is high-quality independent peer-reviewed work; (2) in-vitro fibroblast (a cell that builds collagen) data on palmitoyl tripeptide-5 itself, which is thinner and predominantly supplier-sponsored; and (3) human cosmetic efficacy data for Syn-Coll-containing formulations, which is mostly open-label, split-face, or vehicle-controlled at small sample sizes and generally reported in supplier technical bulletins, cosmetic trade publications, or review articles that cite supplier data.

• Foundational TSP-1 / TGF-β biology (strong) — The Schultz-Cherry / Murphy-Ullrich program (1993–2000) established that TSP-1 non-proteolytically activates latent TGF-β via the KRFK motif binding LAP's LSKL sequence. Crawford et al. (1998, Cell; PMID 9657149) demonstrated physiologic relevance in TSP-1-null mice. This is the biology Syn-Coll is pitched to mimic, and it is real and robust.
• Fibroblast collagen response to TGF-β (strong) — Varga, Rosenbloom & Jimenez (1987, Biochem J; PMID 3501287) established that TGF-β drives a 2–3× enhancement of type I and type III collagen and a 5–8× increase in fibronectin mRNA in cultured normal human dermal fibroblasts, with effects persisting for at least 72 hours after TGF-β removal. This is the cellular-biology foundation for any "stimulate collagen via TGF-β" cosmetic claim, including Syn-Coll's.
• In-vitro Pal-KVK data (thin, predominantly sponsor-originated) — DSM / Pentapharm technical bulletins and derivative trade-journal coverage report that palmitoyl tripeptide-5 upregulates type I collagen synthesis in dermal fibroblast cultures and compares favorably with palmitoyl pentapeptide-4 (Matrixyl) in head-to-head collagen assays. These are not published in indexed peer-reviewed journals as standalone research papers; they appear as supplier claims, conference abstracts, and narrative references within cosmetic-science review articles.
• Human cosmetic efficacy — supplier-sponsored program — A Pentapharm / DSM–sponsored vehicle-controlled clinical assessment commonly cited in trade and review literature tested a Syn-Coll–containing cream against vehicle and against a palmitoyl pentapeptide (a chain of 5 amino acids) comparator over an 84-day regimen in approximately 60 healthy female subjects, with PRIMOS 3D surface topography endpoints. The report describes roughly a 3.5× wrinkle-reduction ratio vs placebo and a ~12% reduction in wrinkle-depth parameters. The raw study has not been reproduced in a peer-reviewed independent venue and is cited primarily in supplier documentation and review articles that accept supplier data at face value.
• Narrative cosmetic-science reviews — Lupo & Cole's 2007 Dermatologic Therapy review "Cosmeceutical peptides" (PMID 18045359) — the most widely cited cosmeceutical-peptide review in dermatology — places palmitoyl tripeptide-5 alongside palmitoyl pentapeptide-4 (Matrixyl) and palmitoyl tripeptide-1 in the "signal peptides" category. More recent review articles (Errante et al., 2020, Front Chem, PMC7662462; subsequent cosmetic-science reviews) similarly catalog Syn-Coll among TSP-1-mimicking cosmetic actives without advancing new independent efficacy data.
• Combination/formulation context — Most published evaluations that include palmitoyl tripeptide-5 test it within multi-peptide cosmetic formulations (e.g., alongside Matrixyl 3000, palmitoyl tripeptide-1, Argireline, and antioxidants) rather than as a monotherapy. This makes any observed efficacy attributable to the ensemble rather than to Syn-Coll specifically and is the main reason independent isolation of Syn-Coll's effect size is difficult.
• No human wrinkle-morphometry RCT in PubMed — A direct PubMed search for "palmitoyl tripeptide-5" as a monotherapy in a vehicle-controlled randomized wrinkle-endpoint trial returns supplier and review coverage but not a standalone peer-reviewed RCT at the rigor level one would expect for a topical retinoid or niacinamide study. This is the single most important evidence-quality caveat for this compound.

Human Data

Human data on Syn-Coll is limited to cosmetic efficacy and tolerance studies — there are no clinical trials of systemic palmitoyl tripeptide-5, because the compound is a topical ingredient by design and no regulatory authority has ever approved or investigated it for systemic use. Specific human-subject evaluations that appear in the literature and supplier documentation:

• Pentapharm / DSM Syn-Coll sponsor study (≈60 subjects, 84 days) — Vehicle-controlled evaluation of a topical formulation containing Syn-Coll against vehicle placebo and against a palmitoyl pentapeptide (Matrixyl-class) comparator cream. PRIMOS 3D optical topography was used to quantify periorbital wrinkle depth and roughness parameters. Reported outcomes: approximately 3.5× wrinkle-parameter improvement vs vehicle and a ~12% reduction in aggregate wrinkle-depth score over 84 days, favoring Syn-Coll over comparator. Study report is primarily available in DSM's Syn-Coll technical bulletin and cited secondarily in cosmetic-science review articles (e.g., Lupo & Cole 2007; more recent DSM product-literature updates). Not indexed as an independent peer-reviewed randomized trial in PubMed.
• Multi-peptide formulation trials — Several independent cosmetic efficacy studies evaluating multi-active formulations that include palmitoyl tripeptide-5 alongside palmitoyl tetrapeptide-7, palmitoyl tripeptide-1, and/or acetyl hexapeptide-8 (Argireline). These report modest but statistically measurable reductions in wrinkle-depth, improvements in dermal density on ultrasound imaging, and improved subject self-assessment. Because the formulations contain multiple actives, these studies do not isolate Syn-Coll's contribution.
• Tolerance and patch-test data — The supplier's safety data sheet reports no skin irritation in a 48-hour human patch test and no sensitization in a human repeat-insult patch test, without giving the concentration tested (DSM safety data sheet, 2017). No independent tolerance study of palmitoyl tripeptide-5 on its own has been published.
• Sensitization risk — The Cosmetic Ingredient Review (CIR) Expert Panel has not assessed palmitoyl tripeptide-5: it is not in CIR's ingredient index, and CIR's 2012 literature review of palmitoyl oligopeptides, which reached no conclusion, found no published irritation or sensitization studies of palmitoyl peptides.
• What is not in the human evidence base — No randomized placebo-controlled monotherapy trial of palmitoyl tripeptide-5 with pre-registered primary wrinkle-morphometry endpoints published in a PubMed-indexed dermatology journal. No histological biopsy studies demonstrating measurable collagen-density change in biopsied skin sections after topical Syn-Coll application. No comparative effectiveness data against topical tretinoin, retinol, or a well-characterized growth-factor serum.

The honest read is that Syn-Coll has been used in finished cosmetic products and tolerated safely by large numbers of consumers for roughly two decades, which is real-world evidence of safety at cosmetic use-levels. Its efficacy as an isolated active is supported by mechanistically coherent supplier-sponsored data and by the robustness of the upstream TSP-1/TGF-β biology, but not by the kind of independent randomized trial portfolio one would expect for a drug candidate.

Reconstitution & Storage

DSM supplies Syn-Coll as a ready-to-use, glycerin-based water solution (DSM safety data sheet, 2017). There is no reconstitution step analogous to injectable peptides. Handling details from the supplier:

→ Calculator — vial-to-syringe math

Side Effects & Risks

Its safety record rests mainly on the supplier's own tests, reported in its safety data sheet (DSM safety data sheet, 2017); PubMed lists no safety study of the peptide on its own. Key considerations:

• Local skin reactions — In the supplier's 48-hour human patch test the product caused no skin irritation (DSM safety data sheet, 2017). No published study gives a rate of skin reactions in use.
• Contact sensitization — The product did not cause sensitization in the supplier's human repeat-insult patch test (DSM safety data sheet, 2017), and PubMed lists no report of allergy to palmitoyl tripeptide-5. The Cosmetic Ingredient Review (CIR) has not assessed it: it is not in CIR's ingredient index, and CIR's 2012 literature review found no published sensitization studies of palmitoyl peptides.
• Use on broken or compromised skin — No study has tested it on wounds, dermatitis or freshly treated skin.
• Theoretical concern — chronic topical TGF-β activation — TGF-β is a central player in fibrotic disease, and TSP-1 is increased in the skin and blood plasma of people with scleroderma (Murphy-Ullrich & Suto, 2018). No study or case report links topical palmitoyl tripeptide-5 to scarring or fibrosis.
• Pregnancy and lactation — No study has tested topical palmitoyl tripeptide-5 in pregnancy or breastfeeding.
• Interaction with retinoids and AHAs — No study has tested it together with retinoids or alpha-hydroxy acids.
• Injection — No study has tested palmitoyl tripeptide-5 by any kind of injection; its supplier identifies its use as an ingredient for skin-care products (DSM safety data sheet, 2017).
• Oral use — No study has tested it by mouth; the supplier's safety data sheet gives only a calculated acute oral toxicity estimate for the product, above 5,000 mg/kg (DSM safety data sheet, 2017).
• Eyes — The supplier's safety data sheet says the product may irritate eyes, and that it was irritating to mucous membranes in an in-vitro assay (DSM safety data sheet, 2017).

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for Syn-Coll, and no study has measured palmitoyl tripeptide-5 in blood. The supplier's tests measured the skin itself: wrinkles by PRIMOS skin-surface imaging (Schagen, 2017) and collagen by skin imaging (dsm-firmenich product page).

Commonly Stacked With

Product labels list palmitoyl tripeptide-5 on its own as well as with other peptides and common skin-care actives. Pairings found on such labels:

Stacking this? Read the receipt →

→ Calculator — vial-to-syringe math

Legal Status

Related Compounds

Cosmetic signal peptides in the same collagen-signaling class:

Next Steps

References

1. Schultz-Cherry S, Murphy-Ullrich JE. Thrombospondin causes activation of latent transforming growth factor-beta secreted by endothelial cells by a novel mechanism. J Cell Biol. 1993;122(4):923-932. doi:10.1083/jcb.122.4.923. PMID: 8349738. (The foundational paper demonstrating non-proteolytic TSP-1 activation of latent TGF-β — the parent mechanism Syn-Coll is designed to mimic.)
2. Schultz-Cherry S, Ribeiro S, Gentry L, Murphy-Ullrich JE. Thrombospondin binds and activates the small and large forms of latent transforming growth factor-beta in a chemically defined system. J Biol Chem. 1994;269(43):26775-26782. PMID: 7929413.
3. Schultz-Cherry S, Lawler J, Murphy-Ullrich JE. The type 1 repeats of thrombospondin 1 activate latent transforming growth factor-beta. J Biol Chem. 1994;269(43):26783-26788. PMID: 7929414.
4. Schultz-Cherry S, Chen H, Mosher DF, Misenheimer TM, Krutzsch HC, Roberts DD, Murphy-Ullrich JE. Regulation of transforming growth factor-beta activation by discrete sequences of thrombospondin 1. J Biol Chem. 1995;270(13):7304-7310. doi:10.1074/jbc.270.13.7304. PMID: 7706271. (Localization of the KRFK activation motif — the native sequence Pal-KVK is designed to mimic.)
5. Crawford SE, Stellmach V, Murphy-Ullrich JE, Ribeiro SM, Lawler J, Hynes RO, Boivin GP, Bouck N. Thrombospondin-1 is a major activator of TGF-beta1 in vivo. Cell. 1998;93(7):1159-1170. doi:10.1016/s0092-8674(00)81460-9. PMID: 9657149. (Genetic demonstration in TSP-1-null mice that the TSP-1 → TGF-β activation axis is physiologically required in vivo.)
6. Ribeiro SM, Poczatek M, Schultz-Cherry S, Villain M, Murphy-Ullrich JE. The activation sequence of thrombospondin-1 interacts with the latency-associated peptide to regulate activation of latent transforming growth factor-beta. J Biol Chem. 1999;274(19):13586-13593. doi:10.1074/jbc.274.19.13586. PMID: 10224129. (Mapping of the reciprocal LAP–LSKL / TSP-1–KRFK binding interaction.)
7. Murphy-Ullrich JE, Poczatek M. Activation of latent TGF-beta by thrombospondin-1: mechanisms and physiology. Cytokine Growth Factor Rev. 2000;11(1-2):59-69. doi:10.1016/s1359-6101(99)00029-5. PMID: 10708953. (Definitive mechanistic review of TSP-1-dependent TGF-β activation.)
8. Murphy-Ullrich JE, Schultz-Cherry S, Höök M. Transforming growth factor-beta complexes with thrombospondin. Mol Biol Cell. 1992;3(2):181-188. doi:10.1091/mbc.3.2.181. (Original biochemical characterization of the TSP-1 / TGF-β complex.)
9. Murphy-Ullrich JE, Suto MJ. Thrombospondin-1 regulation of latent TGF-β activation: a therapeutic target for fibrotic disease. Matrix Biol. 2018;68-69:28-43. doi:10.1016/j.matbio.2017.12.009. (Comprehensive modern review of TSP-1 / TGF-β targeting for disease; PMC6015530.)
10. Varga J, Rosenbloom J, Jimenez SA. Transforming growth factor beta (TGF beta) causes a persistent increase in steady-state amounts of type I and type III collagen and fibronectin mRNAs in normal human dermal fibroblasts. Biochem J. 1987;247(3):597-604. doi:10.1042/bj2470597. PMID: 3501287. (The foundational dermal-fibroblast paper demonstrating TGF-β drives sustained collagen I / III and fibronectin mRNA upregulation — the downstream effect all TGF-β–mimetic cosmetic peptides invoke.)
11. Ignotz RA, Massagué J. Transforming growth factor-beta stimulates the expression of fibronectin and collagen and their incorporation into the extracellular matrix. J Biol Chem. 1986;261(9):4337-4345. PMID: 3456347. (Early demonstration of TGF-β–driven matrix gene expression; co-foundational to Varga 1987.)
12. Lupo MP, Cole AL. Cosmeceutical peptides. Dermatol Ther. 2007;20(5):343-349. doi:10.1111/j.1529-8019.2007.00148.x. PMID: 18045359. (The most widely cited dermatology review of cosmeceutical peptides; positions palmitoyl tripeptide-5 within the signal-peptide class.)
13. Errante F, Ledwoń P, Latajka R, Rovero P, Papini AM. Cosmeceutical Peptides in the Framework of Sustainable Wellness Economy. Front Chem. 2020;8:572923. doi:10.3389/fchem.2020.572923. PMC7662462. (Modern cosmetic-science review cataloging Syn-Coll among TSP-1–mimicking cosmetic actives.)
14. Reszko AE, Berson D, Lupo MP. Cosmeceuticals: practical applications. Dermatol Clin. 2009;27(4):401-416, v. doi:10.1016/j.det.2009.08.005. PMID: 19850190. (Dermatology practice-level overview of cosmeceutical peptide use, including TGF-β–mimetic tripeptides.)
15. Young GD, Murphy-Ullrich JE. Molecular interactions that confer latency to transforming growth factor-beta. J Biol Chem. 2004;279(36):38032-38039. doi:10.1074/jbc.M405658200. PMID: 15208302. (Biochemical characterization of the LAP "latency lasso" that TSP-1 KRFK disrupts.)
16. Young GD, Murphy-Ullrich JE. The tryptophan-rich motifs of the thrombospondin type 1 repeats bind VLAL motifs in the latent transforming growth factor-beta complex. J Biol Chem. 2004;279(46):47633-47642. doi:10.1074/jbc.M404918200. PMID: 15342643. (Identification of the WxxW "docking" motif that orients KRFK on LAP.)
17. Pentapharm / DSM Nutritional Products. Syn®-Coll technical data sheet and efficacy dossier (product literature). DSM Personal Care, Basel, Switzerland. (Supplier-originated dossier describing Syn-Coll's in-vitro collagen upregulation data and the 84-day sponsor-run human wrinkle-morphometry study referenced throughout the cosmetic-science review literature. Not indexed in PubMed.)
18. Cosmetic Ingredient Review Expert Panel. Safety Assessment of Palmitoyl Oligopeptides and Palmitoyl Polypeptides as Used in Cosmetics. Int J Toxicol. CIR Final Report (periodic updates). (Regulatory safety review of the palmitoyl-peptide class, including palmitoyl tripeptide-5.)
19. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
20. Schagen SK. Topical Peptide Treatments with Effective Anti-Aging Results. Cosmetics. 2017;4(2):16. doi:10.3390/cosmetics4020016. (Review; its section on palmitoyl tripeptide-3/5 reports the supplier's in-vivo results: a 10–25 ppm cream with a dose-dependent wrinkle reduction on PRIMOS imaging, and a 60-volunteer, 84-day study of twice-daily use against placebo and a pal-KTTKS cream.)
21. DSM Nutritional Products Ltd. SYN®-COLL safety data sheet according to Regulation (EC) No 1907/2006, product 5038330, version 2.0, revision date 7 November 2017. dsm-firmenich.com/content/dam/dsm-firmenich/perfumery-beauty/personal-care/documents/sds/en/sds-syn-coll-en-gb-11-17.pdf. Read October 4, 2026.
22. dsm-firmenich. SYN®-COLL CB product page. dsm-firmenich.com/en/businesses/perfumery-beauty/beauty-care/products/syn-coll.html. Read October 4, 2026; cited as "2024 version" for its September 25, 2024 text, archived at web.archive.org/web/20240925101924/https://www.dsm-firmenich.com/en/businesses/perfumery-beauty/beauty-care/products/syn-coll.html.

Related Research

• MatrixylCollagen Signal Peptide
• ArgirelineSNAP-25 Mimetic
• SNAP-8Topical Cosmetic / SNARE-Complex Mimetic
• Tripeptide-29Cosmetic Collagen Fragment
• FDA TrackerPCAC voted on 7 of the 12 peptides on July 23–24, 2026; FDA plans a PCAC review of the other 5 before the end of February 2027.